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通过 F-box 蛋白 RAH1 和 RAE1 介导的 STOP1 降解平衡了拟南芥的铝抗性和生长。

Degradation of STOP1 mediated by the F-box proteins RAH1 and RAE1 balances aluminum resistance and plant growth in Arabidopsis thaliana.

机构信息

College of Resources and Environmental Sciences, Nanjing Agricultural University, Nanjing, 210095, China.

Shanghai Center for Plant Stress Biology and National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of Sciences, Shanghai, 200032, China.

出版信息

Plant J. 2021 Apr;106(2):493-506. doi: 10.1111/tpj.15181. Epub 2021 Mar 10.

DOI:10.1111/tpj.15181
PMID:33528836
Abstract

The C2H2-type zinc finger transcription factor sensitive to proton rhizotoxicity 1 (STOP1) is crucial for aluminum (Al) resistance in Arabidopsis. The F-box protein Regulation of AtALMT1 Expression 1 (RAE1) was recently reported to regulate the stability of STOP1. There is a unique homolog of RAE1, RAH1 (RAE1 homolog 1), in Arabidopsis, but the biological function of RAH1 is still not known. In this study, we characterize the role of RAH1 and/or RAE1 in the regulation of Al resistance and plant growth. We demonstrate that RAH1 can directly interact with STOP1 and promote its ubiquitination and degradation. RAH1 is preferentially expressed in root caps and various vascular tissues, and its expression is induced by Al and controlled by STOP1. Mutation of RAH1 in rae1 but not the wild-type (WT) background increases the level of STOP1 protein, leading to increased expression of STOP1-regulated genes and enhanced Al resistance. Interestingly, the rah1rae1 double mutant shows reduced plant growth compared with the WT and single mutants under normal conditions, and introduction of stop1 mutation into the double mutant background can rescue its reduced plant growth phenotype. Our results thus reveal that RAH1 plays an unequally redundant role with RAE1 in the modulation of STOP1 stability and plant growth, and dynamic regulation of the STOP1 level is critical for the balance of Al resistance and normal plant growth.

摘要

对质子根毒性敏感的 C2H2 型锌指转录因子 1(STOP1)是拟南芥耐铝的关键。最近有报道称,F-box 蛋白 Regulation of AtALMT1 Expression 1(RAE1)调节 STOP1 的稳定性。拟南芥中有一个独特的 RAE1 同源物 RAH1(RAE1 同源物 1),但 RAH1 的生物学功能尚不清楚。在本研究中,我们表征了 RAH1 和/或 RAE1 在调节铝抗性和植物生长中的作用。我们证明 RAH1 可以直接与 STOP1 相互作用,促进其泛素化和降解。RAH1 在根冠和各种维管束组织中优先表达,其表达受 Al 诱导并受 STOP1 调控。在 rae1 突变体而非野生型(WT)背景中突变 RAH1 会增加 STOP1 蛋白水平,导致 STOP1 调节基因的表达增加和耐铝性增强。有趣的是,与 WT 和单突变体相比,rah1rae1 双突变体在正常条件下的植物生长减少,而将 stop1 突变引入双突变体背景中可以挽救其植物生长减少的表型。因此,我们的结果表明,RAH1 在调节 STOP1 稳定性和植物生长方面与 RAE1 具有同等冗余的作用,STOP1 水平的动态调节对于铝抗性和正常植物生长的平衡至关重要。

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